Background-Carbon monoxide (CO) is postulated to protect tissues against several types of injuries. We investigated the role of CO in amelioration of cardiac ischemia-reperfusion injury in vivo and the mechanisms involved in it. Methods and Results-Rats inhaled CO (250 ppm, 500 ppm, or 1000 ppm) for 24 hours in a chamber after myocardial ischemia-reperfusion induced by occluding the left anterior descending coronary artery for 30 minutes. Pre-exposure to 1000 ppm of CO significantly reduced the ratio of infarct areas to risk areas and suppressed the migration of macrophages and monocytes into infarct areas, and the expression of tumor necrosis factor (TNF)-␣ in the heart; however, 250 ppm, 500 ppm of CO, or low barometric pressure hypoxia (0.5 atm) did not affect them. Exposure to 1000 ppm CO resulted in the activation of p38 mitogen-activated protein kinase (p38MAPK), protein kinase B␣(Akt), endothelial nitric oxide synthase (eNOS), and cyclic guanosine monophosphate (cGMP) in the myocardium. Inhibition of p38MAPK, PI3kinase, NO, and soluble guanylate cyclase with SB203580, wortmannin, N(G)-nitro-L-arginine methyl ester (L-NAME), and methylene blue, respectively, attenuated the cytoprotection by CO. Conclusion-CO has beneficial effects on cardiac ischemia-reperfusion injury; this effect is mediated by p38MAPK pathway and Akt-eNOS pathway, including production of cGMP.
In the catheter ablation for AF, we found no significant reduction in the 1-year incidence of recurrent atrial tachyarrhythmias by ATP-guided PVI compared with conventional PVI.
12 patients who had histological proven ganglioneuromas were investigated by computed tomography (CT) and magnetic resonance (MR) imaging. CT scans (n = 11), conventional spin-echo MR images (n = 10) and dynamic MR images (n = 5) were acquired. All lesions showed a well defined, oval shape. Five lesions (42%) showed calcification which was punctate in four and coarse in one on CT. CT attenuation was predominantly low in three of 10 (30%) and intermediate in the remaining seven (70%). In all lesions MR signals were mainly of low intensity on T1 weighted images (T1WI) and of high intensity on T2 weighted images (T2WI). Dynamic MR studies in five cases showed a lack of early enhancement but gradual increasing enhancement. One case had a ganglioneuroblastoma component which showed soft-tissue density and coarse calcifications on CT scans, MR images with intermediate intensity on T1WI and T2WI and early enhancement and little washout on dynamic MR images. In conclusion, ganglioneuroma typically shows punctate calcification and low attenuation on CT and marked hyperintensity on T2WI with gradual increasing enhancement on dynamic MR images. If a ganglioneuroma has atypical CT and MR features, coexistence of a malignant component should be considered.
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